b.p. - there is a tie to hypothyroid

[triffid113]

Is anyone else out there trying to control their b.p. w/o drugs? I am extremely drug sensitive...

I had a protocol that worked, but over time I've found it does not work in a bunch of serious situations...namely during allergy seasons (which have lengthened for me since I turned 50), nor does it work following exercise (which RAISES my bp).

In particular I find that allergies use up zinc (I can indeed breathe again if I take enough zinc - 100mg zinc picolinate (which is like 100% more absorbable - if not more - than other forms). So my theory is that allergies destroy nasal skin and it takes zinc to replace skin. (Although zinc lowers IgG, not sure how that figures in). But right or no, it is clear that in the presence of allergies I have insufficient zinc without major augmentation. However it ALSO takes zinc to make thyroxin. So my allergies use up all available zinc (AND POSSIBLY ADDITIONAL ELEMENTS) and my thyroid starts to go south. When that happens...well there are studies now showing a link between SUBCLINICAL hypothyroidism and low GFR (it slows the kidneys). Slowing the kidneys, raises BLOOD PRESSURE (at least in someone genetically disposed, such as me). So if my body makes too much aldosterone I can't get rid of it. Even if my body does not make too much, it adds up because I cannot get rid of it. ok, I get rid of it over night, but then I can't sleep for constantly getting up to pee and I have high blood pressure all day. I have not solved this yet and it's looking like I'm gonna have to go on drugs, but I am so sensitive to drugs I will not be able to stand my life from that moment forward.

If anyone else has tried to control bp w/o drugs I'd like to know your experiences and I'd like to caution you to take your bp every day because there are things we are only discovering that can throw off the best protocol. You could think it pointless to measure as every day you are ok, ok, ok, but 6 months down the road there may be a day you'll find you are NOT ok and there is YET MORE TO BE LEARNED about blood pressure. SInce I am ACE +/+ I have the feeling this is what is going to kill me. My Dad died of his MTHFR 1298AC+/+. I am very leery of +/+.

Just wondered if anyone has b.p. off drugs experiences and info to share.

I find in some notes I took from a defunct holistic training url that vanadium is needed to make thyroxine - I will have to look into this as I am low on vanadium - a byproduct of being from a hereditary diabetic family. Maybe that's why zinc alone doesn't keep my thyroid normal...?

Some studies:

Volume 105, Issue 2, February 2005, Pages 127–149

Zinc metabolism in airway epithelium and airway inflammation: basic mechanisms and clinical targets. A review

Peter D. Zalewski, Ai Q. Truong-Tran, Dion Grosser, Lata Jayaram, Chiara Murgia, Richard E. Ruffin

In addition to basic housekeeping roles in metalloenzymes and transcription factors, dietary zinc (Zn)

is an important immunoregulatory agent, growth cofactor, and cytoprotectant with anti-oxidant,

anti-apoptotic, and anti-inflammatory roles. These properties of Zn are of particular importance

in maintaining homeostasis of epithelial tissues which are at the front line of defense. This review is

about the role of Zn in airway epithelium (AE). The first part focuses on the cellular biology of Zn,

and what is known about its distribution and function in AE. The second part of the review

considers evidence for altered Zn metabolism in asthma and other chronic diseases

of airway inflammation. Important issues arise from a potential therapeutic perspective as to the

optimal ways to monitor circulating and epithelial Zn levels in patients and the most effective

means of supplementing these levels.



Influence of Zinc and Selenium Deficiency on Parameters Relating to Thyroid Hormone Metabolism

A. Kralik, K. Eder, M. Kirchgessner
Institute of Nutrition Physiology, Technical University Munich, Freising-Weihenstephan, Germany
48 weaned male Sprague-Dawley rats with an initial average body weight of 41 g were divided into 4 groups of 12 animals (zinc-deficient; zinc-adequate, pair-fed with zinc-deficient group; selenium-deficient; selenium-adequate) for 40 days. All groups were fed a semisynthetic diet with casein being the source of protein. In the selenium-deficient diet, there was a selenium concentration of 0.038 mg/kg. The other diets were supplemented with Na-selenite in order to adjust the selenium concentration to 0.3 mg/kg. In the zinc-deficient diet, there was a zinc concentration of 4.1 mg/kg. The zinc concentrations in the other diets were adjusted to 45 mg/kg by the addition of zinc-sulfate heptahydrate. Zinc-deficient rats were characterized by a markedly reduced alkaline phosphatase activity in their serum, whilst selenium-deficient rats showed a markedly reduced glutathione peroxidase in serum proving their respective zinc-deficient and selenium-deficient states. Zinc deficiency decreased concentrations of triiodothyronine (T3) and free thyroxine (fT4) in serum by approximately 30% when compared with zinc-adequate controls. The concentration of thyroxine (T4) in serum was not affected by zinc deficiency. Selenium-deficient animals had lower concentrations of T3and T4 than selenium-adequate animals. The concentration of fT4 in serum was not affected by selenium deficiency. The activity of hepatic type I 5′deiodinase was decreased by 67% by zinc deficiency and by 47% by selenium deficiency compared to adequate controls. The study data show that both zinc and selenium deficiency affect the metabolism of thyroid hormones.


American Journal of the Medical Sciences:
October 1999 - Volume 318 - Issue 4 - p 277
Original Articles

Blood Volumes and Renal Function in Overt and Subclinical Primary Hypothyroidism


VILLABONA, CARLES MD; SAHUN, MANUEL MD; ROCA, MANUEL PhD; MORA, JAUME MD; GÓMEZ, NÚRIA MD; GÓMEZ, JOSÉ M. MD; PUCHAL, RAFAEL PhD; SOLER, JOAN MD




Abstract



Introduction: Thyroid dysfunction is associated with marked alterations in cardiovascular and renal functions. In hypothyroidism, myocardial contractility, cardiac output, and oxygen consumption are decreased, whereas peripheral resistance is increased. Methods: We assessed blood volumes and effective renal plasma blood flow (ERPF) and glomerular filtration rate (GFR) in 17 patients with overt primary hypothyroidism and in 15 of these patients when in euthyroid state after substitutive therapy. We performed the same measurements in eight patients with subclinical hypothyroidism. Results: In the hypothyroid state, the plasma volume measured by dilution of 125I-albumin (APV) was higher than the calculated plasma volume (CPV) from packed red cell mass, suggesting an extravascular escape of albumin. After substitutive therapy, the CPV showed a statistical increase (P< 0.05), whereas APV remained unchanged. Both ERPF and GFR increased after thyroxine therapy (p< 0.05). In the subclinical group, blood volumes and renal function were similar to those found in the other group of patients when in the euthyroid state. Conclusions: We conclude that in primary hypothyroidism, ERPF and GFR are low, but that these values improve with substitutive therapy. CPV is a better index of the current plasma volume than APV. The difference between these two parameters suggests that the escape of albumin into the extravascular space in primary hypothyroidism is terminated by treatment. There are no clear abnormalities either in blood volumes or in renal function in subclinical hypothyroidism.

Consistent Reversible Elevations of Serum Creatinine Levels in Severe Hypothyroidism FREE
Stuart H. Kreisman, MDCM; James V. Hennessey, MD
Arch Intern Med. 1999;159(1):79-82. doi:10.1001/archinte.159.1.79.

Background Changes in routine clinical chemical indicators of renal function in the hypothyroid state are not well characterized, and are infrequently discussed in standard internal medicine or subspeciality textbooks.
Patients and Methods We evaluated 24 consecutive patients with iatrogenic hypothyroidism induced prior to radioiodine scanning for monitoring of thyroid carcinoma. Serum creatinine and thyroid function tests were measured prior to, during, and subsequent to the period of induced hypothyroidism.
Results Among 29 episodes with paired prior euthyroid and hypothyroid serum creatinine values, the hypothyroid value was greater in 26 (89.7%), and equal in 3 (10.3%), less in none; the mean hypothyroid value was significantly greater (103 vs 76 µmol/L [1.17 vs 0.87 mg/dL]) (P<.001). Among 36 episodes with paired hypothyroid and subsequent euthyroid serum creatinine values, the hypothyroid value was greater in 33 (91.7%), equal in 2 (5.6%), and less in 1 (2.8%); the mean hypothyroid value was again significantly greater (102 vs 75 µmol/L [1.15 vs 0.85 mg/dL]) (P<.001). There was no significant difference between prior and subsequent euthyroid serum creatinine values. Serum creatinine values above the stated normal range occurred in 6 of 36 hypothyroid episodes.
Conclusions There is a consistent and reversible elevation of serum creatinine values in the hypothyroid state. Frankly abnormal serum creatinine levels will occur in some cases.

J Clin Invest. 1974 October; 54(4): 926–934.
doi: 10.1172/JCI107833
PMCID: PMC301633
Mechanism of Impaired Water Excretion in the Hypothyroid Rat

Dimitrios S. Emmanouel, Marshall D. Lindheimer, and Adrian I. Katz




The ability to excrete an oral water load and the renal diluting mechanism were studied in hypothyroid rats and in age-matched euthyroid controls. Hypothyroid animals excreted a significantly smaller fraction of a 50-ml/kg oral water load than controls, demonstrating the same limited ability to excrete free water as thyroid-deficient man. During hypotonic (0.45%) saline infusion, absolute sodium delivery to the diluting segment and free water clearance were markedly lower in hypothyroid rats. However, both fractional distal sodium delivery and fractional free water clearance were similar in hypothyroid and control animals, suggesting that the reduced absolute free water formation in hypothyroid rats was due to decreased net distal delivery. In support of this hypothesis was the observation that fractional distal sodium reabsorption was equal or higher in thyroid-deficient rats, which indicates that the sodium reabsorptive capacity of the diluting segment was preserved in these animals. The results cannot be attributed to incomplete suppression of antidiuretic hormone (ADH) since they were identical in diabetes insipidus rats, nor to different rates of non-ADH-dependent backflux of filtrate since tissue osmolality and solute concentrations in the cortex, medulla, and papilla were similar in hypothyroid and control rats of both Sprague-Dawley and Brattleboro strains.
The functional integrity of the diluting segment in hypothyroid rats was further demonstrated in experiments in which distal delivery was increased by contralateral nephrectomy or by administration of carbonic anhydrase inhibitors which decrease proximal sodium reabsorption. In both studies, fractional free water clearance increased markedly reaching levels significantly greater than in euthyroid controls.
These results demonstrate that the impaired ability of the hypothyroid rat to excrete a water load is not due to incomplete suppression of ADH or decreased reabsorptive capacity of the diluting segment but results from decreased filtrate delivery to this site secondary to reduced GFR.


Correlation between severity of thyroid dysfunction and renal function


Den Hollander, J. G., Wulkan, R. W., Mantel, M. J. and Berghout, A. (2005), Correlation between severity of thyroid dysfunction and renal function. Clinical Endocrinology, 62: 423–427. doi: 10.1111/j.1365-2265.2005.02236.x

Objective  Renal function is profoundly influenced by thyroid status; however, this has not been studied in detail in human subjects. The purpose of the present study was to determine the relationship between renal function and thyroid status before and after treatment for hypothyroidism and hyperthyroidism, respectively.
Design and patients  In 37 consecutive hypothyroid and 14 hyperthyroid patients renal function as measured by plasma creatinine and glomerular filtration rate (GFR) [based on the modification of diet in renal disease (MDRD) formula] was determined before treatment and after regaining euthyroidism.
Results  Renal function improved significantly during treatment of hypothyroidism and decreased during treatment of hyperthyroidism. There was a strong correlation between the change in thyroid status determined as the ratio log10(fT4 post-treatment/fT4 pretreatment) and the change in renal function as a result of therapy expressed as serum creatinine (r2 = 0·81, P < 0·0001) and estimated GFR (0·69, P < 0·0001).
Conclusion  The kidney is an important target of thyroid hormone action.

 

[triffid113]

Another hiccup in bp control strategies:


Effects of insufficient sleep on blood pressure in hypertensive patients

A 24-h study

Paola Lusardi, Annalisa Zoppi, Paola Preti, Rosa Maria Pesce, Elena Piazza and Roberto Fogari

Am J Hypertens (1999) 12 (1): 63-68.



The influence of acute sleep deprivation during the first part of the night on 24-h blood pressure monitoring (ABPM) was studied in 36 never-treated mild to moderate hypertensive patients. According to a crossover design, they were randomized to have either sleep deprivation or a full night's sleep 1 week apart, during which they were monitored with ABPM. Urine samples for analysis of nocturnal urinary excretion of norepinephrine were collected. During the sleep-deprivation day, both mean 24-h blood pressure and mean 24-h heart rate were higher in comparison with those recorded during the routine workday, the difference being more pronounced during the nighttime (P < .01). Urinary excretion of norepinephrine showed a significant increase at night during sleep deprivation (P < .05). Blood pressure and heart rate significantly increased in the morning after a sleep-insufficient night (P < .05). These data suggest that lack of sleep in hypertensive patients may increase sympathetic nervous activity during the night and the following morning, leading to increased blood pressure and heart rate. This situation might represent an increased risk for both target organ damage and acute cardiovascular diseases. Am J Hypertens 1999;12:63–68 © 1999 American Journal of Hypertension, Ltd.

 

[triffid113]

Ok, well no one has added anything but here is the trail I am following...based on discussion with life extension re: some of my labs, and observation, this is a new type of blood pressure problem I am running afoul of (new for me) I believe. My protocol is still doing something for me because w/o it my bp is 3x as high. However it appears that now the problem is that inflammation causes high blood pressure. Since I already take a high level of antioxidants (translate anti-inflammatories) I am at a bit of a loss, hence the investigation. (Like idk what else to take that is anti-inflammatory or how else to get my CRP back down where it belongs). Life Extension told me there is a tie to blood sugar and diabetes runs in my family. I have shown to be low in some of the blood sugar trace minerals like vanadium and chromium in the past (and kinda neglected that since it caused no effect at the time). I remember reading ibn Life EXtension magazine recently that gamma tocopherol lowers blood sugar immediately after meals (similarly that TMG lowers homocysteine immediately after meals). Since my fasting blood sugar is excellent (80 - which is on the money) and I have indeed found (due to my Dad having been diabetic and having all the paraphernalia) that my blood sugar goes quite high after eating. Also my crp started creeping up (not considered high yet, but no longer low). So I investigated the tie between gamma tocopherol and blood pressure and found this in humans showing gamma tocopherol lowers oxidative stress:


http://www.sciencedirect.com/science/article/pii/S0891584907008210



Free Radical Biology and Medicine

Volume 44, Issue 6, 15 March 2008, Pages 1203–1208



Gamma-tocopherol supplementation alone and in combination with alpha-tocopherol alters biomarkers of oxidative stress and inflammation in subjects with metabolic syndrome



Sridevi Devaraj, Scott Leonard, Maret G. Traber, Ishwarlal Jialal



Metabolic syndrome (MetS) is associated with increased incidence of diabetes and cardiovascular disease (CVD). Prospective clinical trials with alpha-tocopherol (AT) have not yielded positive results. Because AT supplementation decreases circulating gamma-tocopherol (GT), we evaluated supplementation with GT (800 mg/day), AT (800 mg/day), the combination or placebo for 6 weeks alone AT and GT concentrations, biomarkers of oxidative stress, and inflammation in subjects with MetS (n = 20/group). Plasma AT and GT levels increased following supplementation with AT alone or GT alone or in combination. AT supplementation significantly decreased GT levels. Urinary alpha- and gamma-CEHC, metabolites of the respective Ts, also increased correspondingly, i.e., alpha-CEHC with AT and gamma-CEHC with GT supplementation, compared to placebo. HsCRP levels significantly decreased in the combined AT+GT group. LPS-activated whole blood release of IL-1 and IL-6 did not change. There was a significant decrease in TNF with AT alone or in combination with GT. Plasma MDA/HNE and lipid peroxides were significantly decreased with AT, GT, or in combination. Nitrotyrosine levels were significantly decreased only with GT or GT+AT but not with AT compared to placebo. Thus, the combination of AT and GT supplementation appears to be superior to either supplementation alone on biomarkers of oxidative stress and inflammation and needs to be tested in prospective clinical trials to elucidate its utility in CVD prevention.


And then this showing a tie between insulin, blood sugar, triglycerides, and blood pressure NOT weight (THAT is a fallacy as my mother went from a size 16 to size 8 and it did not change her bp):



http://www.sciencedirect.com/science/article/pii/0026049579900180

Metabolism

Volume 28, Issue 6, June 1979, Pages 650–658

Effects of long-term physical training on body fat, metabolism, and blood pressure in obesity

· Marcin Krotkiewskia, b, c,

· Konstantinos Mandroukasa, b, c,

· Lars Sjöströma, b, c,

· Lars Sullivana, b, c,

· Hakon Wetterqvista, b, c,

· Per Björntorp

Twenty-seven women with varying degrees of obesity were physically trained for 6 mo on an ad lib. diet. Body fat changes were positively correlated with the number of fat cells in adipose tissue. Obese women with fewer fat cells decreased in weight during training whereas women with severe obesity and an increased number of fat cells even gained weight. Blood pressure decreased consistently after training. Blood pressure elevation was not associated with body fat mass, nor was a decrease in blood pressure associated with a decrease in body fat or with pretraining blood pressure level. There were, instead, correlations between decreases in blood pressure on the one hand and initial concentrations and decreases in plasma insulin and triglycerides and blood glucose on the other. These results suggest an association between elevated blood pressure and metabolic variables. The possibility of treating and preventing early essential hypertension with methods that also correct the metabolic derangement, such as diet and exercise, should be given high priority in further research.

There is more but I have to go just now

 

[triffid113]

Ok, I guess I am not going to include them, but I found quite a few studies in rats that showed vanadium lowers blood pressure. I should say vanadyl whatever (LIfe Extension kept correcting me - it is NOT plain vanadium and I wouldn't want to misinform anyone - but if you search for vanadium and hypertension you will still find the studies). Also chromium lowers bp.

The thing about THIS kind of hypertension (due to inflammation) is that you cannot feel it. The kind I get genetically (or whatever - the kind taken care of via cal-mag + DHEA - I can feel...it always causes a headache and - actually more - a feeling that even a sneeze could cause a stroke. It does not cause kidney slow down (well over time it would cause kidney malfunction of course)

This kind is more insidious. For me the only symptom is my kidneys slowing down. Kidneys are very sensitive to inflammation. (I know this because my father died in kidney failure and I spent a lot of time talking to various kidney doctors). As well as to low thyroxin.

 

[triffid113]

So tie tie-in is that since my thyroid was low all winter due to allergies I put on weight and INFLAMMATION. That is why the blood sugar aspect of hyperthyroid is particularly bothering me now and was not before. In fact as an allergy goes on, I get 2-3 weeks before my thyroid goes south enough to bother me (I hold the line that long due to zinc ingestion however I am uncomfortable taking any more than I do esp. since surely zinc is not the only thing I am using up albeit it seems to be a major player) and then I start to eat more and I do not have the trace minerals to handle blood sugar. So...idk how much of my kidney problem is due to actual hypothyroid vs. the fact that it makes me eat more and cause blood sugar problems. Or even due to the fact that hypothyroid raises my cholesterol and affects my blood pressure THAT way. (It seems a 3-per hit).

 

[triffid113]

gamma tocopherol lowers IL-6, which is one of the cytokines raised in allergies (I think):

http://www.sciencedirect.com/science/article/pii/S1051227607001124

Journal of Renal Nutrition
Volume 17, Issue 5, September 2007, Pages 296–304

Gamma-Tocopherol and Docosahexaenoic Acid Decrease Inflammation in Dialysis Patients



Jonathan Himmelfarb, MD, Stephen Phinney, PhD, T. Alp Ikizler, MD, Jane Kane, BA, Ellen McMonagle, MS, Guy Miller, MD, PhD

Objective

Increased cardiovascular risk in hemodialysis patients may be related to augmented oxidative stress and inflammation, for which no proven beneficial therapies are available.

Study Design

We examined the effects of gamma tocopherol and docosahexaenoic acid (DHA) administration on inflammation and oxidative stress markers in hemodialysis patients in a randomized, double-blinded, placebo-controlled, clinical trial. Active treatment consisted of capsules containing gamma tocopherol (308 mg) and DHA (800 mg).

Setting

Outpatient dialysis center.

Patients

Seventy maintenance hemodialysis patients.

Main Outcome Measures

Plasma concentrations of interleukin-6 (IL-6) and protein carbonyl content were determined by enzyme-linked immunosorbant assay. C-reactive protein was measured by nephelometry. The F2 isoprostanes were measured by gas chromatography-mass spectrometry. Erythrocyte DHA content was measured by gas chromatography.

Results

Sixty-three patients were enrolled, and 57 completed the study. No serious adverse events were attributed to either active treatment or placebo. In the treatment group, but not in the placebo group, there were significant decreases in IL-6 (21.4 ± 3.5 to 16.8 ± 3.7 pg/mL), white blood cell (WBC) count (7.4 ± 0.3 to 6.9 ± 0.4 103/μL), and neutrophil fraction of WBCs (4.8 ± 0.3 to 4.4 ± 0.3 103/μL), at P < .05 for all. There were no significant changes in plasma concentrations of CRP, F2 isoprostanes, or carbonyls in either group.

Conclusion

Thus, gamma tocopherol and DHA are well-tolerated and reduce selected biomarkers of inflammation in hemodialysis patients. Larger randomized, clinical trials will be required to determine if gamma tocopherol and DHA can reduce cardiovascular complications in hemodialysis patients.

 

[triffid113]

Ah -- this one says gamma tocopherol may protect BH4 from peroxynitrate (ONOO), which preserves the body's ability to make NOS (a vasodilator) and is why it would help blood pressure. I will have to tell Rand56 as he is particulary interested in dodging ONOO. Alas, this is only a hypothesis, but it appears to be based on some studies



Medical Hypotheses

Volume 69, Issue 6, 2007, Pages 1367–1370

Gamma-tocopherol may promote effective no synthase function by protecting tetrahydrobiopterin from peroxynitrite

· Mark F. McCarty

Summary

Oxidation of tetrahydrobiopterin by peroxynitrite in oxidant-stressed endothelium compromises nitric oxide synthase (eNOS) activity while amplifying superoxide production; this mechanism contributes prominently to the endothelial dysfunction that characterizes many common clinical disorders. As a physiological peroxynitrite scavenger, gamma-tocopherol may have the potential to protect tetrahydrobiopterin and thus preserve effective eNOS activity. Indeed, in clinical studies, supplemental gamma-tocopherol has enhanced platelet eNOS activity, and a diet high in gamma-tocopherol-rich walnuts has improved endothelium-dependent vasodilation in hypercholesterolemia. In rodents, gamma-tocopherol is reported to increase arterial expression of eNOS while up-regulating an activating phosphorylation of this enzyme. Although epidemiological efforts to link gamma-tocopherol status with coronary risk have yielded inconsistent findings, this does not rule out the possibility that high intakes of this antioxidant could provide clinical protection. The impact of supplemental gamma-tocopherol on compromised endothelium-dependent vasodilation in various disorders merits examination.

 

[triffid113]

There is a PDF file I can't seem to copy and paste here from Krakow university which says that gamma-tocopherol preserves eNOS (which produces vasodilator NO and thus regulates blood pressure). The title is: Nitric Oxide Synthase Activity in Blood Vessels of Spontaneously Hypertensive rats: Antioxidant protection by gamma-tocopherol.
Newaz et al. Journal of Physiology ad Pharmacology, 2003

 

[triffid113]

In their new compendium book, LEF says that androgen receptor blockers not only lower blood pressure, but also lower inflammation and increase lifespan 20%. I may have to try them but they scare me because DHEA is an androgen and I can't function w/o it (the androgen blockers in flea meds make me feel like I cannot stand for anything to touch me and also invalidate my DHEA so that I have a constant panic attack, etc.

 

[triffid113]

Vitamin E in general helps bp. I wonder how high a dose I can take? I am comfrtble taking 1-1.2g/day. Beyond that is virgin territory...

http://hyper.ahajournals.org/content/39/1/135.short

Hypertension. 2002; 39: 135-141
Scientific Contributions

Enhanced Nitric Oxide Inactivation and Protein Nitration by Reactive Oxygen Species in Renal Insufficiency

Nosratola D. Vaziri, Zhenmin Ni, Fariba Oveisi, Kaihui Liang, Raj Pandian

Chronic renal failure (CRF) is associated with oxidative stress which promotes production of reactive carbonyl compounds and lipoperoxides leading to the accumulation of advanced glycation and lipoxidation end products. Reactive oxygen species (ROS) avidly reacts with nitric oxide (NO) producing cytotoxic reactive nitrogen species capable of nitrating proteins and damaging other molecules. This study tested the hypothesis that CRF results in enhanced ROS-mediated NO inactivation and protein nitration which can be ameliorated with antioxidant therapy. Male Sprague Dawley rats were randomized to CRF (5/6 nephrectomy) and sham-operated controls and fed either a regular diet (vitamin E, 40 U/Kg food) or an antioxidant-fortified diet (vitamin E, 5000 U/Kg food) for 6 weeks. Blood pressure, plasma malondialdehyde (MDA), tissue NO synthase (NOS) isoforms, tissue nitrotyrosine (the footprint of NO interaction with ROS), and vascular tissue NO production were determined. CRF resulted in marked elevations of blood pressure, plasma MDA, and tissue nitrotyrosine abundance, but did not change plasma L-arginine level. This was coupled with depressed vascular tissue NO production and reduced immunodetectable NOS proteins in the vascular, renal, and cardiac tissues. Antioxidant therapy ameliorated the CRF-induced hypertension, improved vascular tissue NO production, lowered tissue nitrotyrosine burden, and reversed downregulations of NOS isoforms. In contrast, antioxidant therapy had no effects in the controls. CRF is associated with oxidative stress which promotes NO inactivation by ROS leading to functional NO deficiency, hypertension, and widespread accumulation of protein nitration products. Amelioration of oxidative stress by high-dose vitamin E enhances NO availability, improves hypertension, lowers protein nitration products, and increases NOS expression and vascular NO production in CRF animals.

 

[Crux]

Hi triff;
Here's an article by Dr. Mark Houston. He's an internist who specializes in hypertension.
He recommends a variety of foods and supplements that have BP lowering effects.
He even describes their actions, such as that of; an Angiotensin Converting Enzyme Inhibitor,(ACEI), or Angiotensin II Receptor Blocker, (ARB), and so on.

I think most of his recommendations are spot on, but some seem odd to me, such as casein and zein.

http://onlinelibrary.wiley.com/doi/10.1111/jch.12188/pdf

 

[triffid113]

Ok, thanks. Let me read that in a sec. I want to add one important thing...WATER. I passed my doctor appointment today (my sister asked me what it means to say that I did not flunk and it basically means that my doctor did not drop me as a patient for failure to comply with taking hypertension drugs). I drank 3 pint bottles of water the day before and 3 the morning of and it lowered my blood pressure to passing range. So...here's the thing...I have to take so many pills that I think it is causing dehydration. Then allergy season comes around, and I have additional bp problems from that due perhaps to inflammation? Well anyway I think I need more water - I have found before one time that dehydration was the cause of high bp (that was on a very hot day). I tried to read up - can't really pin this to a study - except that rats with genetic high bp are found to be less effective at regulating bodily fluids - not just electrolytes. I find several discussions on this from RN's though, such as:
http://www.lisanelsonrd.com/blog/high-blood-pressure-and-dehydration

High Blood Pressure and Dehydration

When you think about water and blood pressure the link between dehydration and low blood pressure probably comes to mind. Dehydration is a potential cause of low blood pressure due to resulting decreased blood volume leading to reduced pressure against artery walls.

However, did you know not drinking enough water can lead to high blood pressure?

When you do not drink adequate water the body will compensate by retaining sodium. That should be a red flag. Sodium is directly related to high blood pressure.
While this sodium retention takes place, the persistent dehydration will lead the body to gradually ‘close’ some of the capillary beds. This leads to increased pressure places on arteries and a rise in blood pressure.





Also I find this by an unknown person:
http://www.buzzle.com/articles/dehydration-and-blood-pressure.html

During dehydration the water levels drop drastically, but the body still needs water for various functions. In this case the essential organs in the body will be given priority for water, whereas the capillaries that supply nutrients to your skin and muscles, are closed. Moreover during dehydration, the water is drawn from the blood to meet the required needs of the essential functions. This lowers the blood volume, in the arteries and veins, which ideally need to be full. Now once this blood is transported to the organs, the blood vessels contract, to keep up with the available volume of blood. A hormone like substance called histamine is produced, which causes the narrowing of the blood vessels. This contraction can cause tension in the blood vessels, which will increase the blood pressure.


(This shows a tie between allergies and high bp...so now I am going to search for hypertension and histamine.)

 

[triffid113]

Thanks Cruz...I printed a copy of tat paper to look at later. Meanwhile I want to say for others that I ran across a referece that low blood volume can be a cause of POTS, for anyone interested in exploring that connection. Maybe you all already know that.

 

[triffid113]

Since hypertension and high cholesterol often go together (not required though) and uncontrolled allergies and high cholesterol DEFINITELY go together (due to allergies wear down the thyroid and low thyroid causes high cholesterol), my cholesterol has been climbing in the past year (now that I have allergies all winter - a long time). My doctor just prescribed berberine. Thought some of you might be interested. Here is one of many studies I find:

http://www.sciencedirect.com/science/article/pii/S0378874106002248
Effects of berberine on diabetes induced by alloxan and a high-fat/high-cholesterol diet in rats

Li-Qin Tanga,Wei Weia, ,Li-Ming Chenb,Sheng Liub
Journal of Ethnopharmacology
Volume 108, Issue 1, 3 November 2006, Pages 109–115

Berberine is the major active constituent of Rhizoma coptidis. The present study was carried out to investigate the effect of berberine on diabetes in rats and its possible mechanisms. Diabetes was induced by tail vein injection with alloxan in Wistar rats. The amount of alloxan administered was 55 mg/kg. Diabetic rats were fed with a high-cholesterol diet. The fasting blood glucose, total cholesterol (TC), triglyceride (TG) and low density lipoprotein-cholesterol (LDL-c), high density lipoprotein-cholesterol (HDL-c), nitric oxide (NO) levels in serum and malondialdehyde (MDA),superoxide dismutase (SOD),glutathione peroxidase (GSH-px) contents in heart tissue were assayed by spectrophotometry. Pancreas samples collected after 3 weeks of alloxan treatment were stained with hematoxylin–eosin (HE) and examined under a light microscope, and scored. Intragastric administration of berberine (100 and 200 mg/kg) .significantly decreased fasting blood glucose levels, serum content of TC, TG, LDL-c, and effectively increased HDL-c, NO level in diabetic rats Furthermore, berberine treatment significantly blocked the increase of MDA, increased SOD and GSH-px levels in diabetic rats. Histopathological scores showed that berberine had restored the damage of pancreas tissues in rats with diabetes mellitus. The results showed berberine significantly inhibited the progression of diabetes induced by alloxan, and the inhibitory effect of berberine on diabetes might be associated with its hypoglycemic effect, modulating lipids metabolic effects and its ability to scavenge free radical.


So as I read that, berberine normalizes the lipid profile, improves blood pressure, cures a diseased pancreas, raises glutathione peroxidase, and scavenges some free radicals! I may not be able to take it tho' -- we'll see, because it lowers blood sugar and although I have elevated blood sugar post meals, I have a normal fasting glucose - on the money at 80 - and I have had lifelong low blood sugar. (Now I find that if I get low blood sugar it means I forgot or was delinquent on a dose of DHEA so, with DHEA I may be able to tolerate berberine). I have a very hard time keeping my thyroid functional during allergy season and at those times I need help in every way, including with cholesterol.

 

[triffid113]

This one is also of interest as it says it does not work via statins (and thus does not affect CoQ10 levels the way statins do):
http://www.nature.com/nm/journal/v10/n12/abs/nm1135.html

Nature Medicine 10, 1344 - 1351 (2004)
Published online: 7 November 2004; | doi:10.1038/nm1135
Berberine is a novel cholesterol-lowering drug working through a unique mechanism distinct from statins

Weijia Kong1, 5, Jing Wei2, 5, Parveen Abidi3, 5, Meihong Lin3, Satoru Inaba3, Cong Li3, Yanling Wang4, Zizheng Wang2, Shuyi Si1, Huaining Pan2, Shukui Wang2, Jingdan Wu2, Yue Wang4, Zhuorong Li1, Jingwen Liu3& Jian-Dong Jiang1, 4

We identify berberine (BBR), a compound isolated from a Chinese herb, as a new cholesterol-lowering drug. Oral administration of BBR in 32 hypercholesterolemic patients for 3 months reduced serum cholesterol by 29%, triglycerides by 35% and LDL-cholesterol by 25%. Treatment of hyperlipidemic hamsters with BBR reduced serum cholesterol by 40% and LDL-cholesterol by 42%, with a 3.5-fold increase in hepatic LDLR mRNA and a 2.6-fold increase in hepatic LDLR protein. Using human hepatoma cells, we show that BBR upregulates LDLR expression independent of sterol regulatory element binding proteins, but dependent on ERK activation. BBR elevates LDLR expression through a post-transcriptional mechanism that stabilizes the mRNA. Using a heterologous system with luciferase as a reporter, we further identify the 5' proximal section of the LDLR mRNA 3' untranslated region responsible for the regulatory effect of BBR. These findings show BBR as a new hypolipidemic drug with a mechanism of action different from that of statin drugs.


Here's a study which mentions dosages used for diabetes (perhaps less if diabetes is not present?):

Berberine has been shown to regulate glucose and lipid metabolism in vitro and in vivo. This pilot study was to determine the efficacy and safety of berberine in the treatment of type 2 diabetes mellitus patients. In study A, 36 adults with newly diagnosed type 2 diabetes mellitus were randomly assigned to treatment with berberine or metformin (0.5 g 3 times a day) in a 3-month trial. The hypoglycemic effect of berberine was similar to that of metformin. Significant decreases in hemoglobin A1c (from 9.5% ± 0.5% to 7.5% ± 0.4%, P < .01), fasting blood glucose (from 10.6 ± 0.9 mmol/L to 6.9 ± 0.5 mmol/L, P < .01), postprandial blood glucose (from 19.8 ± 1.7 to 11.1 ± 0.9 mmol/L, P < .01), and plasma triglycerides (from 1.13 ± 0.13 to 0.89 ± 0.03 mmol/L, P < .05) were observed in the berberine group. In study B, 48 adults with poorly controlled type 2 diabetes mellitus were treated supplemented with berberine in a 3-month trial. Berberine acted by lowering fasting blood glucose and postprandial blood glucose from 1 week to the end of the trial. Hemoglobin A1c decreased from 8.1% ± 0.2% to 7.3% ± 0.3% (P < .001). Fasting plasma insulin and homeostasis model assessment of insulin resistance index were reduced by 28.1% and 44.7% (P < .001), respectively. Total cholesterol and low-density lipoprotein cholesterol were decreased significantly as well. During the trial, 20 (34.5%) patients experienced transient gastrointestinal adverse effects. Functional liver or kidney damages were not observed for all patients. In conclusion, this pilot study indicates that berberine is a potent oral hypoglycemic agent with beneficial effects on lipid metabolism.

oops - sorry! I accidentally closed the session with the study before I copied the name and authors of the study!

 

[brenda]

trifid

I have had HBP (plus high cholesterol and raised blood sugar, high histamine with IC ) in the past and found that freshly juiced celery brings it down a treat. Celery is high in sodium. However, I do not like to use a remedy like this or anything, without searching for the cause of the problem and I have nailed it down to my diet.

The significant changes the last 6 months have been, cutting dairy, (significant) sugar, nightshade veggies, eggs, cutting fat right down, increasing whole grains - brown rice especially, (no unfermented wheat) and reducing animal protein to 3-4 small servings a week. I use hemp protein. Histamine levels have reduced as sneezing has gone down considerably.

My bp is now 120/85 without using celery juice. This is despite being over 60, overweight and CDS in the family. I get my cholesterol and sugar checked this week.

If you dont mind me asking, what are you eating and are you still exposing yourself to pesticides?

 

[triffid113]

Well....I had a protocol that works PERFECTLY if not during allergy season. I have ACE +/+ gene as well as NOS +/- and at least one other that caused hypertension...that +/+ is pretty hard to get around...and that does not include whatever genes cause allergies - mine are the worst my allergist has ever seen. I have not been able to get around histamine causing high bp yet.

I also found exercise causes high bp for me. So - to those pigs who tell me that "all you have to do is exercise and your bp will go down" (no pigs like that here of course), it's not true. In fact a study even backs up what I found - it says exercise lowers platelet aggregation on NONhypertensives, but NOT SUFFICIENTLY in hypertensives, causing clotting and strokes.

So I mentioned I am going to try UC-II to prevent allergy to joint collagen during exercise to see if that helps. But Also I am intending to look into anti-PAF substances. Frankly I eat healthily and I am not willing to modify my diet in the way that you list...for instance I greatly crave milk products which contain tyrosine and I figure I must need tyrosine, which afterall is needed for thyroid and adrenal glands and to make dopamine. I eat eggs each and very day and never will I change that as it is a complete protein and I do not feel well when I do not eat eggs for breakfast. Anyhow I have tried going off milk and eggs before and it did nothing for my allergies. I hear from life extension that going off wheat completely takes care of high blood pressure. Well I followed a celiac diet for 2 years and it did not take care of my allergies...although it DID take care of PMS. I was not hypertensive then as I was younger and my hormones took care of it. I am frustrated that with hormone replacement I obviously cannot get back to the exact hormone levels I had before to take care of bp at all times although DHEA does the trick for me except for during hayfever or exercise, both of which are autoimmune reactions.

 

[triffid113]

I wouls appreciate if anyone would nominate things they know to be anti-PAF (platelet aggregating factor). I will check celery seed. I do know celery seed is good for bp. I had already solved my bp with DHEA so didn't choose that method, but now I am finding circumstances where DHEA is insufficient.

 

[Lynn]

triffid113

When that happens...well there are studies now showing a link between SUBCLINICAL hypothyroidism and low GFR (it slows the kidneys). Slowing the kidneys, raises BLOOD PRESSURE (at least in someone genetically disposed, such as me). So if my body makes too much aldosterone I can't get rid of it. Even if my body does not make too much, it adds up because I cannot get rid of it. ok, I get rid of it over night, but then I can't sleep for constantly getting up to pee and I have high blood pressure all day. I have not solved this yet and it's looking like I'm gonna have to go on drugs, but I am so sensitive to drugs I will not be able to stand my life from that moment forward.

I am also looking at the connection between hypothyroidism and high blood pressure. I have inherited high blood pressure as well. Dr. Cheney told me that CFS was probably helping to keep my blood pressure in check.

In the past couple of months I have made two major changes. First is to take high dose thiamine (vitamin B-1) daily. (This has been a miracle for me). The second was to start a diet called "The Perfect Health Diet" (a low carb/high fat lots of plants/some meat kind of diet). All in all I am feeling pretty good as long as I don't overdo it and end up in PEM.

Then after about two weeks on the B-1 I ended up with chronic hives and my blood pressure went up. I was worried that the B-1 or the diet was causing it. The researcher for the high dose B-1 protocol said that he has not seen hives as a reaction in the years that he has been studying it.

So I got on the internet and finally found some anecdotal postings connecting hives and hypothyroidism. Then I found out that B-1 can lower one's thyroid production. So I asked my doctor to try upping my dosage of Armour thyroid and the hives are going away within a few days. It also seems to be bringing my blood pressure back down. I didn't realize there was a connection between hypothyroidism and high blood pressure.

The B-1 has changed my life. I am not cured but I am getting some quality of life back. I am glad that the Armour Thyroid may help with the blood pressure. I didn't want to have to choose between doing a few things in my life and having a stroke!

Lynn

 

[triffid113]

Um, hives are an allergic reaction and cortisol (made by the adrenal gland) takes down allergic reactions. There is a tie between the thyroid and the adrenal gland, but I don't know what it is. I only know that w/o enough thyroid hormone one cannot make enough adrenal hormones. So during allergies, I might try upping my DHEA and/or thyrocsin (well I already up the zinc and I crave milk products containing tyrosine so maybe it's the trace elemnts in thyrocsin that I need more of), or else I could try taking dried adrenal hormone (I hate taking that because it's very hard for me to get the dose right, but I'll do it if it helps my allergy problems!). I have blood work that clearly shows my thyroid going out during allergy season (and as a side effect, my cholesterol rising). I do not have a thyroid doctor and doubt I could find one to help me until my TSH >5.5 (which it has been, but I have severe symptoms way before then). It recovers after allergy season. Well, thanks for that very useful bit of info!